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特发性胎儿生长受限的病因研究
引用本文:Zhao J,Wu LF. 特发性胎儿生长受限的病因研究[J]. 中华妇产科杂志, 2004, 39(5): 329-333
作者姓名:Zhao J  Wu LF
作者单位:100026,首都医科大学附属北京妇产医院产科
摘    要:目的 通过研究胎儿生长受限(FGR)的相关因素,探讨特发性FGR的可能病因。方法63例孕期拟诊为FGR的孕妇,按新生儿出生体重分组,小于该孕龄平均体重第10百分位数的29例为研究组A;大于该孕龄平均体重第10百分位数的34例为研究组B。另选择25例分娩正常体重新生儿的孕妇为对照组。3组孕妇于孕期检测50 g葡萄糖负荷试验(50 g GCT)、75 g葡萄糖耐量试验(75 g OGTT)、瘦素、血红蛋白水平及红细胞压积、感染系列、抗心磷脂抗体(ACA)、脐动脉收缩期与舒张期(S/D)比值。于分娩时检测脐血瘦素、C肽、胰岛素水平及病毒系列、染色体。结果 (1)研究组A孕妇的空腹血糖和餐后3 h血糖分别为(3.8±0.6)mmol/L和(4.5±1.1)mmol/L,脐血瘦素、C肽、胰岛素水平分别为(7.3±5.2)ng/ml、(0.5±0.3)nmol/L、(2.3±1.3)mU/L,脐动脉S/D比值、母、儿巨细胞病毒(CMV)感染率、ACA-IgM阳性率及无症状菌尿症发生率分别为3.06、20.7%、24.1%、44.8%和62.1%。(2)研究组B孕妇的空腹血糖和餐后3 h血糖分别为(4.4±0.7)mmol/L和(4.6±1.1)mmol/L,脐血瘦素、C肽、胰岛素水平分别为(13.2±11.3)ng/ml、(0.7±0.4)nmol/L、(4.3±3.3)mU/L,脐动脉S/D比值、母、儿CMV感染率、ACA-IgM阳性率及无症状菌尿症发生率分别为2.63、2.9%、0、5.9%和44.1

关 键 词:特发性胎儿生长受限 病因 血糖 巨细胞病毒感染 血流速度
修稿时间:2003-09-09

Study of the causes of fetal growth restriction with unclear etiologies
Zhao Jun,Wu Lian-fang. Study of the causes of fetal growth restriction with unclear etiologies[J]. Chinese Journal of Obstetrics and Gynecology, 2004, 39(5): 329-333
Authors:Zhao Jun  Wu Lian-fang
Affiliation:Department of Obstetrics, Affiliated Beijing Obstetrics and Gynecology Hospital, Affiliated Capital University of Medical Sciences, Beijing 100026, China.
Abstract:OBJECTIVE: To investigate different factors related to fetal growth restriction (FGR) and to find out the possible causes of FGR with unclear etiologies. METHODS: Sixty-three women who were suspected of FGR during pregnancy between March 2002 and March 2003 were included in this study. Their age, body mass index (BMI) before pregnancy, and gestational weeks were recorded at the time when they were first diagnosed. Haemoglobin levels, haematocrit (HCT), TORCH, anticardiolipin antibody (ACA), 50 gram glucose challenge test (50g GCT), 75 gram oral glucose tolerance test (75g OGTT), leptin levels, systolic/diastolic (S/D) ratio by color doppler monitor and chlamydia trachomatis (CT) were detected and urine culture was done in these groups during the same period. The gestational week, birth weight, body length and the gender were recorded at the delivery period. The FGR group was then divided into two subgroups according to the birth weights: study A group whose birth weights were lower than 10th% of the birth weights at the given gestational weeks (29 cases) and study B group whose birth weights were beyond 10th% (34 cases). The chromosome, leptin, C-peptide, insulin and TORCH of umbilical blood were measured at delivery. The other 25 normal pregnant women were included as control and the same tests were performed accordingly. RESULTS: The fasting glucose and the third hour's glucose of 75 gram oral glucose tolerance test of study A were (3.8 +/- 0.6) mmol/L and (4.5 +/- 1.1) mmol/L. The fetal leptin, C-peptide, and insulin were (7.3 +/- 5.2) ng/ml, (0.5 +/- 0.3) nmol/L and (2.3 +/- 1.3) mU/L. The S/D ratio of umbilical artery, maternal and fetal infection rate of CMV, positive rate of ACA-IgM and the rate of asymptomatic bacteriuria were 3.06, 20.7%, 24.1%, 44.8% and 62.1% respectively. The fasting glucose and the third hour's glucose of 75 gram oral glucose tolerance test of study B were (4.4 +/- 0.7) mmol/L and (4.6 +/- 1.1) mmol/L. The fetal leptin, C-peptide, and insulin were (13.2 +/- 11.3) ng/ml, (0.7 +/- 0.4) nmol/L and (4.3 +/- 3.3) mU/L. The S/D ratio of umbilical artery, maternal and fetal infection rate of CMV, positive rate of ACA-IgM and the rate of asymptomatic bacteriuria were 2.63, 2.9%, 0%, 5.9% and 44.1% respectively. The fasting glucose and the third hour's glucose of 75 gram oral glucose tolerance test in control were (4.3 +/- 0.7) mmol/L and (5.3 +/- 1.2) mmol/L. The fetal leptin, C-peptide, and insulin were (20.5 +/- 12.0) ng/ml, (1.0 +/- 0.4) nmol/L and (6.3 +/- 4.0) mU/L. The S/D ratio of umbilical artery, maternal and fetal infection rate of CMV, positive rate of ACA-IgM and the rate of the asymptomatic bacteriuria were 2.80, 0, 0, 0 and 24.0% respectively. All these items were significantly higher in study A than those in the control (P < 0.05). There was no significant difference between the study B and the control in all the items. CONCLUSIONS: Many factors may play a role in the pathogenesis of FGR, including the maternal blood glucose level, the ability for fetus to use the glucose, the infection of some microorganisms, insufficiency of the blood supply and the autoimmunity of the mother. Finding out the possible causes of FGR and managing them accordingly may improve the outcomes of the fetus.
Keywords:Fetal growth retardation  Blood glucose  Cytomegalovirus infections  Antibodies   anticardiolipin  Umbilical arteries  Blood flow velocity
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